THEORETICAL PHYSIOLOGY 3

G.M. O’Brien, Human Biology (Physiology), University of New England, NSW 2351, Australia gobrien@metz.une.edu.au

Abstract Orgasmic Gushing: where does the fluid come from and how is it produced?, GM O’Brien, TheorPhysiol 3:draft(2000) There are three sexual fluids from women: lubrication (e.g. transudation of fluid across the mucosa of the vagina, and mucus from the greater vestibular glands); female ejaculation (from paraurethral glands); and gushing. Orthodox western medicine and physiology does not yet have a standardized description or explanation for the third, gushing. The present paper proposes that the gushing fluid is a filtrate of plasma, produced by the mechanism known as transudation. This is an additional application for the transudation mechanism, after the well accepted roles in lubrication of the vagina, and in generating serous fluids. The present model proposes that the fluid released in a gush arises from the ventral wall of the vagina due to the presence there of increased surface area of mucosa, dilated arterioles, pressurized venous and lymphatic plexuses, and compression provided by muscle contraction during orgasm. Keywords: orgasm, vagina, gushing, female ejaculation, sex fluids.

Some cultures recognize three sexual fluids from women including for example Tao Zen writers Chia and Chia (1986 pp. 51-52), or Trukese and other Micronesian cultures described in works cited by Sevely (1987, p.68). Orthodox western medicine and physiology recognize two of these sexual fluids. The first, lubrication, consists of mucous secretions from the greater vestibular (formerly Bartholin's) glands and transudation of fluid across the mucosa of the vagina. The second, termed female ejaculation, consists of secretions from the paraurethral (formerly Skene's) glands released through the urethra and paraurethral ducts to the vulva at sexual climax in some women. The third is known in some circles as gushing.

Since Grafenberg's description of the "erotic zone ... on the anterior wall of the vagina" (Grafenberg 1950), and Ladas, Whipple and Perry's (1982) presentation of the broader biology of the G-spot, a reasonable understanding has been developed of the anatomy and physiology of the paraurethral glands and female ejaculation. Confusion still arises however when the paraurethral glands and female ejaculation are used in attempts to explain all expulsions during female orgasm, as in Sevely's (1987) detailed review. Gushing is a separate phenomenon. When the two events, female ejaculation and gushing, are sufficiently understood it should be possible to re-examine many published accounts of female orgasmic expulsions, classify each as either female ejaculation or gushing, and thereby derive much more clear-cut data for each than is currently available.

Gushing is described as thin, watery fluid, with little or no colour, taste, smell or residue. The volume released seems to vary between a few drops, to tens of millilitres to a seemingly limitless volume (Sevely e.g. 126 mL, p.92). The release may occur just once during a coital session, or may occur repeatedly with a series of climax events. When large quantities are released repeatedly some women report indications of dehydration symptoms. The fluid may be released in a gush, that may be projected away from the body in a spurting stream, or may flow, seep or trickle without force. As with female ejaculation, gushing does not occur in all women, and in those who do report the phenomenon it does not occur during all sessions of intercourse i.e. it is an irregular and unpredictable biological event.

The present paper proposes that the gushing fluid is a filtrate of plasma, produced by the mechanism known as transudation. It is proposed that the fluid released in a gush arises from the ventral wall of the vagina due to the presence there of rich vascular supply, a dense venous plexus, loose connective tissue, and a permeable epithelial membrane. The pattern of flow, described as various forms of gushing, results from a sudden increase in tissue fluid content or pressure that probably results from of a wave of vasodilation, reinforced by muscle contractions.

This model resolves some of the problems that have hampered acceptance and understanding of the phenomenon of gushing. There has been no organ in the external genital tract known to be capable of producing fluid, on demand, in such quantity. Glands as small as the paraurethral glands cannot. If instead of 'on demand' it was produced over a period of time it would need to be stored somewhere in a vesicle or bladder, but no such structures have been reported by anatomists. No ducts have been found draining into the vagina and yet most descriptions indicate the fluid seems to arise from somewhere on the ventral wall of the vagina, apparently associated with stimulation of the G-spot. Some observers however have interpreted the fluid as arriving from the urethra, or being delivered directly into the vestibule. The model resolves the problem of absence of a storage vessel, by proposing fluid is produced 'on demand'. The problem of 'what organ would be capable of such fluid production' is resolved in the description below, of arteriolar and capillary exchange mechanisms.

The model of gushing deriving by transudation is expanded under three headings:

The vaginal wall has several layers: adventitia or serosa; muscularis; and mucosa. The mucosa consists of a lamina propria of loose connective tissue and a very permeable stratified squamous epithelium.

On the "epithelial surface are two median longitudinal ridges, one anterior and the other posterior. From these vaginal columns numerous transverse bilateral rugae extend, divided by sulci of variable depth, giving an appearance of conical papillae which are ... especially well developed before parturition." (Williams et al. 1989 p.1445). Many anecdotal reports regarding gushing refer to these rugae on the ventral vaginal column.

Loose connective tissue (also called areolar connective tissue) is described as "like a collapsed sponge this tissue contains innumerable potential spaces ... capable of becoming enlarged and distended with fluid" (Bloom and Fawcett 1968 p.131). The wall of the vagina is richly supplied by arteries which dilate during arousal, under parasympathetic cholinergic neural control; as a result the lamina propria becomes oedematous. The veins and lymph vessels draining the vaginal wall are organized as networks i.e. a venous plexus and a lymphatic plexus.

The blood supplying the vaginal walls arrives from the internal iliac artery in a number of branches, notably the vaginal branches from the uterine artery, and the internal pudendal artery. The vaginal arteries anastomose to form a longitudinal median azygous artery on the ventral surface and another on the dorsal surface of the vagina, feeding the mucosa (Williams et al. 1989).

Engorgement of the vaginal arteries during arousal and filling of the venous plexus causes oedema of the mucosa and transudation for lubrication. The present paper posits that changes in the transudation accompanying orgasm cause gushing.

Transudation is filtration of water, electrolytes, and some proteins from plasma, across a membrane - usually a serous membrane. The vaginal mucosa is unusual in exhibiting transudation without being a serous membrane. Serous membranes are found in the pericardium, pleura, and peritoneum, where a fine film of serous fluid acts as a surfactant-type lubricant. The fluid that diffuses onto the vaginal mucosa during vasocongestion also provides this type of friction modification during sexual intercourse, especially in combination with mucus secreted from the cervical and greater vestibular glands. At rest a small quantity diffuses onto the mucosal surface to maintain hydration. During arousal the lamina propria becomes oedematous and substantial quantities diffuse onto the surface, providing sufficient lubrication for intercourse. At orgasm, an additional increase in diffusion can result in free liquid flowing into the vagina or even gushing out of the vagina.

When the feeder arteries and arterioles dilate the tissue spaces in the lamina propria fill with fluid. When capillary pressure is increased around serous membranes the rate of transudation across the membrane increases in direct proportion to the increase in pressure (e.g. Stewart et al. 1997). From this it can be predicted that an increase in interstitial hydrostatic pressure at orgasm would lead to a predictable and measurable increase in transudation into the vagina during the orgasm.

The chemical composition of gushing fluid needs to be compared with that of serum, plasma, urine, female ejaculate, and transudate collected from the same subjects under similar conditions. Levin (1980) reported the lubricating fluid to be a modified plasma transudate; this needs to be repeated before, during and after orgasm. In the meantime its physiological source can be predicted.

We are looking for a mechanism that can deliver a large quantity of fluid across a membrane in a short time. In biological systems, increases in diffusion are achieved by (a) an increase in surface area across which the flux is occurring; (b) an increase in the driving force which, in this case, is a gradient of hydrostatic pressure; or by (c) increasing the diffusion coefficient by, for example, altering the permeability of the membrane.

Already the surface area of the ventral wall of the vagina is large due to the presence of rugae i.e. folds in the mucosa. If movements or contractions caused these rugae to flatten at the time of orgasm then perhaps more epithelium would be exposed for diffusion. An alternative way to increase the surface area available for transudation would be if additional regions of mucosa were suddenly perfused or placed under hydrostatic pressure at about the time of orgasm. The result of this would be that additional tissue spaces would be filled, a greater surface area of mucosa would deliver fluid to the vaginal lumen and thus the overall rate of transudation may increase from "lubrication" to "gushing".

Transudation occurs across a permeable membrane. It basically consists of the water content of plasma, or an electrolyte solution, which moves by bulk flow-type flux when vasocongestion occurs. The pressure gradient would be increased by increased arterial pressure or rate of inflow of blood; increased venous pressure or disruption to outflow of blood or lymph; or squeezing of the tissue spaces as could occur during contractions of skeletal muscle, smooth muscle, or myoepithelial cells dispersed through the lamina propria.

Increased venous pressure increases transudation at serosal membranes such as the pleura or pericardium, so it can be predicted that it would have a major impact in the vagina also. Certainly venous pressure increases during the vasocongestion that causes erection. Thus transudation sufficient for lubrication accompanies erection. What would cause the additional flow called gushing? There would need to be sudden increases in tissue interstitial pressure. Hydrostatic pressure results from an imbalance between inflow and outflow. Hence any sudden increase in inflow that was not matched with an increased outflow would significantly elevate hydrostatic pressure in the tissue spaces, increasing flux across the mucosal wall. In the pericardium this mechanism is tested systematically by elevating myocardial venous pressure and measuring increases in epicardial transudation /pericardial effusion (Stewart et al. 1997).

i) What would cause a sudden increase in inflow? Inflow is provided via the longitudinal median unpaired arteries of the vagina and thence arterioles of the mucosa. A wave of hyperpolarization such as that causing release of nitric oxide would temporarily decrease arteriolar tone and increase flow into the capillaries feeding the interstitial fluid of the vaginal wall. Nitric oxide has a characteristically brief action before being metabolized, thus a spurt or gush of fluid would be released as a discrete event. The presence of nitric oxide pathways and mechanisms has been confirmed in human male corpus cavernosum and corpus spongiosum (Hedlund et al. 2000) but has presumably not been examined in female tissues.

The skin flush that often characterizes an orgasmic episode is achieved by a sudden wave of peripheral vasodilation (reminiscent of hot flushes). Is gushing a localized outcome of "vaginal flushing"? A sex flush of the vagina? Such vasodilator effects are possibly mediated via cholinergic sympathetic outflow from the anterior hypothalamus (sympathetic vasodilator system, Guyton and Hall 2000) as occurs to cause the sudden "flush" and sweating when a fever reaches its "crisis" (Guyton and Hall 2000). However, parasympathetic mechanisms are also possible. Rapid and copious fluid flow occurs in the stomach in response to a long vagovagal reflex. In this (Guyton and Hall 2000) sensory information is transmitted in the vagus nerve, to the brainstem, and back to the stomach also in the vagus nerves. The reflexes are initiated by distention of the stomach mucosa, and also by tactile stimulation of the surface of the stomach mucosa. This gastric secretion can also be initiated by signals from the brain, especially from the limbic system. These reflex components bear remarkable similarity with the phenomena of interest in the vagina (!) except that vaginal reflexes would act via sacral synapses.

ii) Reduced outflow also increases interstitial pressure and thus transudation. Tonic contractions of the vaginal wall could easily close the venous plexus and prevent the egress of blood. In a study of oxytocin secretion during orgasm, Carmichael et al. (1987) observed large fluctuations in blood flow with each phasic contraction of genital musculature. The blood flow was monitored using anal photoplethysmography (Carmichael et al. 1987). The mechanism being referred to here is observed readily in the lung where, if venous or lymphatic drainage fails causing even slight increase in interstitial pressure, tissue fluid crosses into the alveolar air space causing pulmonary oedema (Guyton and Hall 2000).

iii) In addition to shutting down the veins and lymphatics, contractions of the vaginal wall would squeeze the mucosal "sponge"; this would raise interstitial pressure during orgasm. It would squeeze fluid out, and into the vaginal lumen. This could be achieved by contractions of the smooth muscle of the walls of the vagina, or by contractions of the surrounding skeletal muscles. Vaginal plethysmography, used to monitor vasocongestion of the vagina, show slight decreases in vasocongestion associated with contractions of pubococcygeus muscles whether they occur during orgasm (Perry 1999a) or during Kegel exercises (Perry 1999b) and this is consistent with fluid being squeezed out of the tissue during the contractions.

Rapidity of fluid flux across a membrane is greatly enhanced if the membrane becomes thinner or more permeable. Capillary permeability can be altered neurally by inducing slight changes in electrical membrane potential of the capillary endothelial cells. Water and electrolyte secretion by glands of the gastrointestinal tract probably occurs by parasympathetic activation, causing hyperpolarization of cell membranes and chloride influx, ultimately driving water and electrolyte flux on the luminal side of the epithelial cells (Guyton and Hall 2000).This mechanism is used to increase flow through cholinergically innervated gastric and salivary glands (Guyton and Hall 2000) and can induce massive changes in rates of fluid flow. At times, changes in rate of flux of fluid across membranes due to changes in membrane permeability can compromise homeostasis. Loss of large volumes of fluid due to transudation through skin that has been rendered permeable by burns or radiation can be life threatening.

Thus, changes in permeability would be capable of delivering the quantities of fluid observed during orgasmic gushing, so this possibility needs to be included if evidence of changes in permeability comes to light.

Expulsion of the gushing fluid can occur with or without significant momentum. The mechanisms that expel the fluid are probably separate from the mechanisms that produce the fluid. The most likely source of propulsion is contraction of vaginal musculature and associated perineal muscles especially the pubococcygeus muscles that are typically involved at orgasm. This would be assisted by general bearing down movements, and by contraction of myoepithelial cells through the loose connective tissue.

As described in the preceding section though, these contractions could also be contributing to production of the fluid by pressurizing the venous plexus and squeezing the mucosa.

The ventral wall is so wrinkled that it is effectively two to three times as thick as the dorsal wall (de Graaf 1672, translated by Jocelyn and Setchell 1972) and has a commensurately larger surface area. It is not known whether the ventral column also has more reactive arterioles, or more voluminous venous plexus, separately controlled permeability, or is more susceptible to squeezing by surrounding tissues than the dorsal column. The latter is probable given the proximity of the urethra embedded in the ventral wall and its anchoring of the external urethral sphincter on the ventral wall.

Ducts opening onto the wall of the vagina or urethra have occasionally been described, notably by de Graaf (1672). Most of these are probably lacunae, or pit-like recesses in the mucosa, rather than ducts from glands. The lacunae add to the surface area draining into the lumen. They are not thought to be connected to the paraurethral glands which are ducts surrounded with secretory cells. It seems from some descriptions that both the urethra and vagina have some of these, and therefore both the urethra and vagina could give rise to some transudate at orgasm. This would certainly add to the difficulty of accurately determining which fluids originated from the urethra and which from the vagina, leading to many authors and observers trying to prove that either one or the other is responsible for orgasmic expulsions, when probably each is a source - the urethra being the primary conduit for female ejaculate and the vagina being the primary conduit for gushing.

To add to the difficulty, the urethra seems to occupy a variable position at the peak of arousal - closer to the vaginal meatus. It seems that in some people the vestibule becomes a true receptacle, with the urethra, vagina and ducts all opening into the temporary chamber. This image fits better with the word 'vestibule' than the relatively flat, two-dimensional presentation of the vestibule in the unaroused state.

The model proposed here, in summary, is that gushing probably results from a sex flush washing through the vagina, increasing blood input to the mucosa, accompanied by contractions of the vagina that increase the pressure in the venous plexus; these factors combine to increase transudation across the mucosa. Transudation is probably re-inforced or enhanced by the contractions effectively squeezing fluid out of the lamina propria and lacunae, and sometimes forcing the fluids out of the vagina under pressure.

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